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Essay on An Overview of Multiple Sclerosis

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An overview of the chronic inflammatory demyelinating disease:
Multiple sclerosis

BACKGROUND
The central nervous system (CNS) comprises grey matter, which contains neuron cell bodies and white matter, which contains the nerve axons. Most of the nerve axons are concentrically wrapped around by lipid-rich biological membrane, known as the myelin sheath. In the CNS, myelin is produced by oligodendrocyte. a type of glial cell. (Pfeiffer et al., 1993). These electrical insulating, multilamellar membranes significantly increase the electrical resistance, in which to prevent leakage of electrical currents from the axons, as well as decrease electrical capacitance to reduce the ability of the axons to store electrical energy (Shivane & …show more content…

It is suggested by previous studies that the damage of the myelin sheath in MS involves the activation of inflammatory factors including the CD4+ T cells, CD8+ T cells, B cells, macrophages and microglia cells (Luccinetti et al., 1996; Lassmannet al., 2012). However, whether the immune response triggers the onset of MS, or is a consequence of the disease process is currently not clear. Interestingly, several recent studies suggested that the prevalence rate of MS is significantly increased with latitude, which implies that not only the geographical (environmental) differences but racial and ethnic differences may play a role in the worldwide MS distribution (Rosati, 2001; Simpson et al., 2011).

CLINICAL FEATURES
MS is usually occurs at age of 15 to 55 with the average onset at about 30 years of age. Women are twice more likely than men to develop this debilitating autoimmune disease (Love, 2006). Due to the heterogeneity of the disease, where it can affects many sites of the CNS such as the brain cortex, brainstem, spinal cord as well as the optic nerve, thus the clinical symptoms of MS are widely ranged.

Most MS patients start with the development of transient sensory loss due to the demyelination of the dorsal column, which may progress to motor symptoms including limb muscles weakness or muscle spasticity due the demyelinationg of the upper motor fibres such as corticospinal and corticobulbar tracts. Leg

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